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Cardiovascular primary prevention in 2016

KinsaraAbdulhalim J

University for Health Sciences-King Abdul Aziz Medical City, Department of Cardiology-Jeddah, Kingdom of Saudi Arabia.

DOI: 10.15761/JIC.1000154

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Abstract

Cardiovascular disease remains the leading cause of death despite improved therapy in treating coronary artery disease.Reduction of risk factors has been consistently leading to better outcome.  In addition it was cost effective and can be practiced in community based clinics and hospitals.We discuss the different aspects and mode of primary intervention.

Keywords

primary prevention; cardiovascular risk;Aspirin; statin

Cardiovascular primary prevention in 2016

Cardiovascular disease remains the leading cause of death in the developed countries and is estimated by the year 2030 to be the leading cause of death in the developing countries. This mainly due to increase in the major CVD risk factors like diabetes, hypertension, smoking and hyperlipidemia, which account for 80 % of all CVD deaths worldwide.

There is growing evidnce of the genetic role , Genetic factors identified from genome-wide association studies have provided insights into genetic pathways involved in the causal pathway for atherosclerotic cardiovascular disease. A single genetic trait may ineffectively evaluate the pathway of interest, and it may not account for other complementary genetic pathways that may be activated at various stages of the disease process or evidence-based therapies that alter the molecular and cellular milieu [1].

preliminary research has found a connection between DNA methylation, histone modifications, RNA-based mechanisms and the development of CVD like atherosclerosis, cardiac hypertrophy, myocardial infarction, and heart failure [2].

Mendelian randomization data strongly suggest that hypertriglyceridemia causes atherosclerotic cardiovascular disease, and so triglyceride level-lowering is now more strongly recommended to address the residual CVD risk than has been the case in earlier published guidelines [3].

A number of dietary factors have been associated with modifying CVD risk factors. One such factor is dietary fibre which may have a beneficial association with CVD risk factors. Randomised controlled trials  showed reductions in total cholesterol and LDL cholesterol with increased fibre intake, and reductions in diastolic blood pressure. There were no obvious effects of subgroup analyses by type of intervention or fibre type at short term [4].A study in China showed that substantial health gains occurred from implementation of population-wide dietary salt reduction policies. Most health benefits from any dietary salt reduction program would be realized in adults with hypertension[5].

In a  cohort, associations of calcium intake and mortality varied by sex. For women, total and supplemental calcium intakes are associated with lower mortality, whereas for men, supplemental calcium intake >/=1000 mg/d may be associated with higher all-cause and CVD-specific mortality[6].

Vascular erectile dysfunction is a powerful marker of increased   cardiovascular risk. However, current guidelines lack specific recommendations on the role of the evaluation of vascular erectile dysfunction on cardiovascular risk assessment, as well on the risk stratification strategy that such group should undergo [7].

Cardiovascular disease also has an inflammatory component . Patients with inflammatory arthritis have increased risk of cardiovascular diseases compared with the general population [8].

Not only the diversity of rsik are challanging but also the results showed that the degree of control of risk factors is still low, especially in variables such as smoking and Diabetes Mellitus.

Screening programmes can potentially identify people at high cardiovascular risk and reduce cardiovascular disease morbidity and mortality. However, there is currently not enough evidence showing clear clinical or economic benefits of systematic screening-like programmes over the widely practised opportunistic risk assessment of CVD in primary care settings.  nine randomised controlled trials that assessed the effects of systematic risk assessment has no statistically significant effects on clinical endpoints but only some favourable effects on cardiovascular risk factors[9].

The use of troponin as prognostic biomarker for the primary assessment of cardiovascular risk in asymptomatic patient has been described. the newer generations of high-sensitivity cardiac troponin assays can detect 10-fold lower concentrations of troponin, raisng the potential value troponin in the prevention and management of asymptomatic cardiovascular disease[10].

The use of health behavior change techniques and theory in technology-enabled interventions targeting risk factors and indicators for cardiovascular disease (CVD) prevention and treatment. The most frequently used behavior change techniques were self-monitoring and feedback on performance. Half of the intervention studies named a theory/model - most frequently Social Cognitive Theory, the Trans-theoretical Model, and the Theory of Planned Behavior/Reasoned Action [11].

Pharmacists' attitudes appeared to be the strongest predictor of CVD support provision. The theory of Planned Behavior  framework was useful in identifying "subjective norms" and "pharmacists' beliefs" as key constructs of community pharmacists' attitudes. Community pharmacies would be able to provide such an advanced clinical service if they strongly believed that this was an acknowledged part of their scope of practice, had adequate infrastructure and employed sufficient numbers of pharmacists with appropriate and relevant knowledge[12].

Aspirin use had its dilemma. laboratory and clinical response to aspirin therapy in patients with different conditions and settings are diverse. This difference in aspirin response necessitates a personalized, tailored aspirin therapy to maximize the benefit and minimize the risk of aspirin [13].

Only modest reductions in CV events and mortality have been observed with once-daily aspirin treatment in patients with diabetes, including patients with a previous CV event, perhaps because of disparity between aspirin pharmacokinetics and diabetes-related platelet abnormalities.Once-daily aspirin irreversibly inactivates platelets for only a short duration (acetylsalicylic acid half-life, approximately 15-20 minutes), after which time newly generated, active platelets enter the circulation and weaken aspirin's effect. Platelets from patients with diabetes are more reactive and are turned over more rapidly than platelets from normal individuals; the short inhibitory window provided by once-daily aspirin may therefore be insufficient to provide 24-h protection against CV events. Alternative conventional aspirin regimens (e.g. higher daily dose, twice-daily dosing, combination with clopidogrel) and newer formulations (e.g. 24-h, extended-release) have been proposed to overcome the apparent limited efficacy of conventional aspirin in patients with diabetes; however, tolerability concerns and limited clinical efficacy data need to be taken into account when considering the use of such regimens [14].

An average daily dose of 100mg of coated aspirin seems more likely to confer favorable preventive effects on death and cancer, with higher doses more appealing for CVD prevention and lower doses better tolerated[15].

Because of the lack of data in patients 80 years of age and older, it is difficult to make a decision on the initiation of aspirin therapy in this population. Additional research is necessary to better balance the risk versus benefit of this treatment option[16].

Statin therapy was associated with a reduction in MACE and all-cause mortality among participants without clinical CVD but with asymptomatic peripheral arterial disease, regardless of its low CVD risk. The absolute reduction was comparable to that achieved in secondary prevention[17].

In order to prevent the increase in CVD, it has been proposed to develop a low-cost polypill containing four to five generic drugs with known effectiveness in the reduction of the CVD. This polypill has now been tested in 15 studies between 2011 and 2015 for the primary and secondary prevention of CVD and stroke with fairly good results[18].

Community level factors have been linked to health outcomes,Strong Hearts, Healthy Communities aims to reduce CVD morbidity and mortality, improve quality of life, and reduce the health care burden in communities. The client-centred approach, which was embedded in a local community setting, using a web-based health risk assessment that tailored feedback and linkage to regional health management and lifestyle providers proved feasible, and successful. Participating in the health risk assessment elicited actual behaviour change[19].

References

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  2. Voelter-Mahlknecht S (2016) Epigenetic associations in relation to cardiovascular prevention and therapeutics.  Clin Epigenetics 8: 4. [Crossref]
  3. Brinton EA (2016) Management of Hypertriglyceridemia for Prevention of Atherosclerotic Cardiovascular Disease.  Endocrinol Metab Clin North Am 45: 185-204. [Crossref]
  4. Hartley L, May MD, Loveman E, Colquitt JL, Rees K (2016) Dietary fibre for the primary prevention of cardiovascular disease.  Cochrane Database Syst Rev 1: CD011472. [Crossref]
  5. Wang M, Moran AE, Liu J, Coxson PG, Penko J, et al. (2016) Projected Impact of Salt Restriction on Prevention of Cardiovascular Disease in China: A Modeling Study.  PLoS One 11: e0146820. [Crossref]
  6. Yang B, Campbell PT, Gapstur SM, Jacobs EJ, Bostick RM, et al. (2016) Calcium intake and mortality from all causes, cancer, and cardiovascular disease: the Cancer Prevention Study II Nutrition Cohort.  Am J Clin Nutr 103: 886-894. [Crossref]
  7. Shah NP, Cainzos-Achirica M, Feldman DI, Blumenthal RS, Nasir K, et al. (2016) Cardiovascular Disease Prevention in Men with Vascular Erectile Dysfunction: The View of the Preventive Cardiologist.  Am J Med 129: 251-259. [Crossref]
  8. van den Brekel-Dijkstra K, Rengers AH, Niessen MA, de Wit NJ, Kraaijenhagen RA (2016) Personalized prevention approach with use of a web-based cardiovascular risk assessment with tailored lifestyle follow-up in primary care practice - a pilot study.  Eur J Prev Cardiol 23: 544-551. [Crossref]
  9. Dyakova M, Shantikumar S, Colquitt JL, Drew CM, Sime M, et al. (2016) Systematic versus opportunistic risk assessment for the primary prevention of cardiovascular disease.  Cochrane Database Syst Rev 1: CD010411. [Crossref]
  10. Hoff J, Wehner W, Nambi V (2016) Troponin in Cardiovascular Disease Prevention: Updates and Future Direction.  Curr Atheroscler Rep 18: 12. [Crossref]
  11. Winter SJ, Sheats JL, King AC (2016) The Use of Behavior Change Techniques and Theory in Technologies for Cardiovascular Disease Prevention and Treatment in Adults: A Comprehensive Review.  Prog Cardiovasc Dis. [Crossref]
  12. Puspitasari HP, Costa DS, Aslani P, Krass I (2016) An explanatory model of community pharmacists' support in the secondary prevention of cardiovascular disease.  Res Social Adm Pharm 12: 104-118. [Crossref]
  13. Kim J, Becker RC (2016) Aspirin dosing frequency in the primary and secondary prevention of cardiovascular events.  J Thromb Thrombolysis: 1-12. [Crossref]
  14. Bell DS (2016) Aspirin in the prevention of cardiovascular events in patients with diabetes.  Postgrad Med 128: 180-190. [Crossref]
  15. Lotrionte M, Biasucci LM, Peruzzi M, Frati G, Giordano A, et al. (2016) Which Aspirin Dose and Preparation Is Best for the Long-Term Prevention of Cardiovascular Disease and Cancer? Evidence From a Systematic Review and Network Meta-Analysis.  Prog Cardiovasc Dis . [Crossref]
  16. Sarbacker GB, Lusk KA, Flieller LA, Van Liew JR (2016) Aspirin Use for the Primary Prevention of Cardiovascular Disease in the Elderly.  Consult Pharm 31: 24-32. [Crossref]
  17. Ramos R, García-Gil M, Comas-Cufí M, Quesada M, Marrugat J, et al. (2016) Statins for Prevention of Cardiovascular Events in a Low-Risk Population With Low Ankle Brachial Index.  J Am Coll Cardiol 67: 630-640. [Crossref]
  18. Chrysant SG, Chrysant GS (2016) Usefulness of the Polypill for the Prevention of Cardiovascular Disease and Hypertension.  Curr Hypertens Rep 18: 14. [Crossref]
  19. Shen J, Shang Q, Tam LS (2016) Targeting inflammation in the prevention of cardiovascular disease in patients with inflammatory arthritis.  Transl Res 167: 138-151. [Crossref]

Editorial Information

Editor-in-Chief

Massimo Fioranelli
Guglielmo Marconi University

Article Type

Opinion Article

Publication history

Received:February 28, 2016
Accepted: March 14, 2016
Published: March 18,2016

Copyright

©2016KinsaraAbdulhalim J,This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Citation

KinsaraAbdulhalim J (2016) Cardiovascular primary prevention in 2016, J IntegrCardiol,1: DOI: 10.15761/JIC.1000154

Corresponding author

KinsaraAbdulhalim J

Department of cardiology, King Saud Bin Abdulaziz University for Health Sciences, COM, King Abdul Aziz Medical City-WR, King Faisal Cardiac Center, Jeddah, Saudi Arabia

E-mail : kinsaraaj@ngha.med.sa

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